Abstract

Aims People whose birthweights were towards the lower end of the normal range are at increased risk of coronary heart disease. This is attributed to foetal programming through malnutrition, but the cause of the malnutrition is unknown.

Methods and results We studied 6975 men born in Helsinki during 1934–44. Their size at birth was recorded. Babies who later developed coronary heart disease tended to have a low ponderal index (birthweight/length3). Three different placental phenotypes predicted the disease. In primiparous mothers who were short, having below median height, the hazard ratio for the disease was 1.14 (95% confidence interval 1.08–1.21, P< 0.0001) for each centimetre increase in the difference between the length and breadth of the placental surface. In tall mothers whose body mass index was above the median, the hazard ratio was 1.25 (1.10–1.42, P= 0.0007) per 40 cm2 decrease in the surface area. In tall mothers whose body mass index was below the median, the hazard ratio was 1.07 (1.02–1.13, P= 0.01) per 1% increase in the placental weight/birthweight ratio.

Conclusions Three different combinations of maternal and placental size predicted coronary heart disease. The mother's body size determines the availability of nutrients and is linked to the development and function of the placenta, reflected in its shape and size. We speculate that variations in three processes of normal placental development lead to foetal malnutrition. The processes are (i) implantation and spiral artery invasion, (ii) growth of the chorionic surface, and (iii) compensatory expansion of the chorionic surface.